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Identification and characterization of regulatory Long Non-coding RNAs on the Schistosoma mansoni genome through NGS strategies and systems approach

Grant number: 14/24560-8
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): March 01, 2015
Effective date (End): January 15, 2017
Field of knowledge:Biological Sciences - Biochemistry
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Sergio Verjovski Almeida
Grantee:Elton José Rosas de Vasconcelos
Home Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Schistosomes are flatworm flukes that cause the infectious and parasitic disease known as schistosomiasis. They are blood parasites widely distributed around the world with a high importance for Public Health and studies in the field of Molecular Parasitology. The genome of Schistosoma mansoni (etiologic agent in Brazil), which was completely sequenced in 2009, has a size of 363 Mb and over eleven thousand genes were already mapped. These static data pose the even greater challenge of understanding the molecular dynamics responsible for the peculiar features of the parasite biology. Post-transcriptional control of gene expression events, such as modulation of mRNA alternative splicing and silencing by RNAi, as well as epigenetic events such as histone modifications, are present in Schistosoma and, as in other higher eukaryotes, it is believed that a variety of regulatory non-coding RNAs (ncRNAs) mediate such reactions. Next Generation Sequencing (NGS) strategies, like RNA-Seq, have revealed the presence of a wide variety of ncRNAs in the genomes of several organisms. These assays are able to generate a large volume of data that are prone to computational analyses that seek to reveal key biological information about gene expression and its regulation. The present proposal is to conduct in silico experiments aimed at assessing the non-protein coding transcriptome content hidden in the large amount of information obtained through RNA-Seq in Schistosoma. With that, beyond identifying / corroborating novel non-coding elements, with emphasis on long ncRNAs (lncRNAs), the proposal has a major focus on their association with gene regulation mechanisms of the parasite, providing a holistic overview of systems that merge non-coding content with what is encoded into proteins and their interrelated regulatory pathways. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
PEREIRA, ADRIANA S. A.; AMARAL, MURILO S.; VASCONCELOS, ELTON J. R.; PIRES, DAVID S.; ASIF, HUMA; DASILVA, LUCAS F.; MORALES-VICENTE, DAVID A.; CARNEIRO, VITOR C.; ANGELI, CLAUDIA B.; PALMISANO, GIUSEPPE; FANTAPPIE, MARCELO R.; PIERCE, RAYMOND J.; SETUBAL, JOAO C.; VERJOVSKI-ALMEIDA, SERGIO. Inhibition of histone methyltransferase EZH2 in Schistosoma mansoni in vitro by GSK343 reduces egg laying and decreases the expression of genes implicated in DNA replication and noncoding RNA metabolism. PLoS Neglected Tropical Diseases, v. 12, n. 10 OCT 2018. Web of Science Citations: 2.
VASCONCELOS, ELTON J. R.; MESEL, VINICIUS C.; DASILVA, LUCAS F.; PIRES, DAVID S.; LAVEZZO, GUILHERME M.; PEREIRA, ADRIANA S. A.; AMARAL, MURILO S.; VERJOVSKI-ALMEIDA, SERGIO. Atlas of Schistosoma mansoni long non-coding RNAs and their expression correlation to protein-coding genes. DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION, JUL 9 2018. Web of Science Citations: 0.
VASCONCELOS, ELTON J. R.; DASILVA, LUCAS F.; PIRES, DAVID S.; LAVEZZO, GUILHERME M.; PEREIRA, ADRIANA S. A.; AMARAL, MURILO S.; VERJOVSKI-ALMEIDA, SERGIO. The Schistosoma mansoni genome encodes thousands of long non-coding RNAs predicted to be functional at different parasite life-cycle stages. SCIENTIFIC REPORTS, v. 7, SEP 5 2017. Web of Science Citations: 9.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.